Embodiments of the present invention generally relate to loss of atrial transport in the heart, and more specifically to methods and systems for detecting, treating and collecting diagnostic data regarding accelerated junction rhythms (AJR) and accelerated idioventricular ventricular rhythms (AIVR).
Implantable medical devices are well known in the art. They include implantable pacemakers which provide stimulation pulses to a heart to cause a heart, which would normally or otherwise beat too slowly or at an irregular rate, to beat at a controlled normal rate. They also include cardioverters and defibrillators which detect when the atria and/or the ventricles of the heart are in tachycardia arrhythmia or fibrillation, and apply anti-tachycardia pacing therapy and/or cardioverting or defibrillating electrical energy to the heart to restore the heart to a normal rhythm. Implantable medical devices may also include the combined functionalities of a pacemaker and a defibrillator.
Implantable medical devices sense cardiac activity for monitoring the cardiac condition of the patient in which the device is implanted. By sensing the cardiac activity of the patient, the device is able to provide cardiac stimulation therapy when it is required. In a healthy heart, the sinoatrial node (SA node) serves as the natural pacemaker of the heart. It is a group of specialized myocardial cells located on the posterior wall of the upper right atrium at the junction between the atrium and the superior vena cava. It initiates electrical impulses in the heart's myocardium at a more rapid rate than other myocardial cells.
The atrioventricular node (AV node) transmits electrical signals from the atria to the ventricles. It is a small concentration of specialized conductive tissue at the base of the atrial septum. The AV node serves an important role in maintaining atrioventricular synchrony, the sequence of an atrial depolarization followed by a ventricular depolarization after an appropriate conduction time (AS-VS interval). Maintenance of atrioventricular synchrony enhances cardiac output and the loss of it (loss of atrial transport) reduces cardiac output. If the SA node fails, the AV node is capable of serving as an intrinsic back-up pacemaker of the heart. However, the cardiac rate, under such circumstances, is generally lower than normal (40 to 60 beats per minute) and is without atrial transport. In special circumstances, the junctional pacemaker may accelerate and usurp control from an otherwise normal sinus node. In the setting of sinus node dysfunction for which a single-chamber atrial or a dual-chamber pacemaker was implanted, the junctional focus may accelerate and usurp control from the otherwise normally functioning pacemaker.
Accelerated junctional rhythms may occur as a consequence of AV nodal ablation, intrinsic disease involving the atrioventricular node also called the AV junction and commonly labeled “junctional pacemaker” or “junctional focus”, as a consequence of metabolic imbalance or as a side effect of a multiplicity of medications.
Hence, patients with SA node dysfunction or who have had their AV node ablated generally have a demand pacemaker to regulate their heart rhythm. While such devices do regulate cardiac rhythm, these patients can experience accelerated junctional rhythms which may then inhibit the artificial pacemaker. While the normal rate of a junctional focus is between 40 to 60 bpm and is dominated by the sino-atrial node which commonly discharges at a more rapid rate (60 to 100 bpm), the accelerated junctional rhythm (AJR) may occur at faster rates than normal and usurp control from the sinus node. The junctional rates accelerate due to a multiplicity of causes including intrinsic disease in the junctional focus, parasympathetic withdrawal or increased sympathetic stimulation. When this focus usurps control from the sinus node or the pacemaker, the faster intrinsic rhythm will be sensed by the pacemaker causing it to inhibit. The result is a loss of atrial transport. This abnormal rhythm may be associated with retrograde conduction to the atrium. In both circumstances, hemodynamics may be compromised resulting in significant symptoms for the patient. Also, under these conditions, the implanted demand pacemakers may be unable to provide assistance as the higher rate of the junctional focus may cause the pacemaker or ICD to be inhibited.
A similar rhythm, but arising from a ventricular focus, is termed accelerated idioventricular rhythm (AIVR). It will have similar consequences with respect to compromising hemodynamics and for the patient who has a dual-chamber pacemaker, result in its inhibition. This rhythm may also be associated with retrograde conduction.
As a group, these rhythms may be labeled as a ventricular complex with loss of atrial transport VCLAT. Hence, functionally, a third VCLAT is sinus rhythm with a marked first degree AV block. In the absence of pacing, a marked first degree AV block may allow the native P wave to coincide with the previous ST-T wave associated with the conducted R wave limiting or even eliminating atrial transport (atrial contraction contributing to ventricular filling) resulting in an under-filled ventricle, a drop in stroke volume and cardiac output and the atria contracting against a closed mitral and tricuspid valve forcing system and pulmonary congestion. In the setting of a dual-chamber pacemaker, this can result in a rhythm labeled Repetitive Non-Reentrant Ventriculo-Atrial Synchrony (RNRVAS) where the native P-wave coincides with the Post-Ventricular Atrial Refractory Period (PVARP) thus allowing for delivery of an atrial output pulse. The atrial output pulse itself is ineffective because the atrial tissue is physiologically refractory in response to the native P wave. During episodes of accelerated junctional rhythms (AJR) or an accelerated idioventricular rhythm (AIVR), there will be a loss of atrial transport and even retrograde conduction. The patients may become symptomatic. This is not uncommon in patients with sinus node dysfunction. The junctional focus responds to increases in sympathetic tone, caused by, for example, physical exertion or any etiology of stress including emotional upset. Throughout the present application, AJR, AIVR and first degree AV block will be collectively referred to as ventricular complex with loss of atrial transport or VCLAT. AIVR rhythms occur in association with other disease states involving the ventricle such as cardiomyopathy, ischemic heart disease and as a side-effect of various medications. As such, an acceleration of the junctional rhythm (meaning both rhythms) may occur at physical rest and/or exercise. Present generation implantable medical devices (pacemaker or ICD) do not have a unique algorithm to detect, treat and collect diagnostic data for patients with VCLAT rhythms (AJR or AIVR or marked first degree AV block).
In each of the above discussed rhythms, there is an intrinsic ventricular depolarization effectively inhibiting the pacemaker; yet each is associated with the loss of an optimal AV delay compromising cardiac function.